The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, People's Republic of China.
Heart Center, Department of Cardiovascular Medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Curr Drug Targets. 2023;24(13):1009-1022. doi: 10.2174/1389450124666230907115831.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new type of oral hypoglycemic drugs that exert a hypoglycemic effect by blocking the reabsorption of glucose in the proximal renal tubules, thus promoting the excretion of glucose from urine. Their hypoglycemic effect is not dependent on insulin. Increasing data shows that SGLT2 inhibitors improve cardiovascular outcomes in patients with type 2 diabetes. Previous studies have demonstrated that SGLT2 inhibitors can reduce pathological myocardial hypertrophy with or without diabetes, but the exact mechanism remains to be elucidated. To clarify the relationship between SGLT2 inhibitors and pathological myocardial hypertrophy, with a view to providing a reference for the future treatment thereof, this study reviewed the possible mechanisms of SGLT2 inhibitors in attenuating pathological myocardial hypertrophy. We focused specifically on the mechanisms in terms of inflammation, oxidative stress, myocardial fibrosis, mitochondrial function, epicardial lipids, endothelial function, insulin resistance, cardiac hydrogen and sodium exchange, and autophagy.
钠-葡萄糖共转运蛋白 2（SGLT2）抑制剂是一种新型的口服降糖药，通过抑制近曲小管对葡萄糖的重吸收，从而促进葡萄糖从尿液中排出，发挥降糖作用。其降糖作用不依赖于胰岛素。越来越多的数据表明，SGLT2 抑制剂可改善 2 型糖尿病患者的心血管结局。既往研究表明，SGLT2 抑制剂可减少有或无糖尿病的病理性心肌肥厚，但确切机制尚待阐明。为阐明 SGLT2 抑制剂与病理性心肌肥厚的关系，以期为未来的治疗提供参考，本研究就 SGLT2 抑制剂减轻病理性心肌肥厚的可能机制进行了综述。我们特别关注了炎症、氧化应激、心肌纤维化、线粒体功能、心外膜脂质、内皮功能、胰岛素抵抗、心脏氢钠交换和自噬等方面的机制。
